Biology Of Tooth

Movement

By
Dr. Aditya Barman Dr.Samit Mondal
Dr.Sankhya Ghosh PGT (s)1st year
Department of Orthodontics
Guru Nanak Institute of Dental Science
&research
 Introduction
Tooth movement by orthodontic force
application is characterized by remodeling
changes in the dental and par dental tissue ,
including the dental pulp, periodontal ligament
alveolar bone and gingiva. These tissue , when
exposed to varying degrees of magnitude,
frequency and duration of mechanical
loading ,express extensive macroscopic and
microscopic changes
It is the only form of movement where solid
object moves in a solid media
 History
Prominent Roman physician Celsus (25 BC-
50 BC) was the first person in the history of
to advocate tooth movement by using
finger pressure .
The modern era dentistry begin in earnest
in 1728 AD with publication of first of the
first comprehensive book on dentistry by
Fauchard (1678-1761) which described a
procedure of Instant orthodontics where
he aligned ectopically erupted incisors by
bending the alveolar bone.
From text book on Biological mechanisms of tooth movement
By V. Krishnan and Z. Davidovitch first edition2009
 History Continued
Fauchard Described an orthodontic appliance
using silk or silver ligatures to malposed teeth
in to new position and Pelican pliers that were
used for instant alignment of incisors,.
Hunter (1728-1793) in 1778, explained that
the teeth might moved by applied force cause
bone moves out of the way of pressure
Delabarre in 1815 reported that orthodontic
forces cause pain and swelling of paradental
tissue

From text book on Biological mechanisms of tooth movement By V.

Krishnan and Z. Davidovitch first edition2009
 History Continued
Farrar in year 1888 hypothesized that
orthodontic forces moved teeth by bending
of the alveolar bone, and/or by causing
Resorption of the bone. And advocated
application of heavy forces to the in order to
move them rapidly.
Carl Sandstedt an Austrian Dentist (1904-
1905) was the first one to prepare a
Histological section examination of
othodontically treated teeth of dog in the
Journal Einige Beitrge zur Throrie der
Zahregulierung . Nord Tandlaeg
Tidskr,5,236,6,1
From text book on Biological mechanisms of tooth movement By
V. Krishnan and Z. Davidovitch first edition2009
 History Continued
Sandsted observed the stretching of
Periodontal ligament in the tension
site and narrowing of this tissue in
the pressure sites. New alveolar bone
formation was seen in the former
locations, and necrosis (hyalinization)
and bone Resorption in the later site.

From text book on Biological mechanisms of tooth movement By V.

Krishnan and Z. Davidovitch first edition2009
 History Continued
(1911-1912), Oppenheimn a reported tooth movement
in pre adolescent Baboon resulting in complete
transformation of entire alveolar process. After
histological examination. Paving the way for orthodontic
force effects spread beyond the limits of PDL
Schwarz (1932) He added a term Optimal force in
smaller magnitude than that capable of occluding PDL
capillary with this it would lead to necrosis of
surrounding tissue and slow down the velocity of tooth
movement.
Schwarz opinion was supported by K.Reitan And Kvam
in 1971
K.Reitan And Kvam (1971 )favored the use of light
intermittent forces , as they cause minimal amount of
tissue damaged and cell death also nature of tissue
response differs from species to species.

a- Oppenheim A (1911/12) Tissue changes, particularly of the bone,

incident to tooth movement American journal of Orthodontic, 35,113-32
Tooth supporting structures- Periodontium
Periodontium is a
connective tissue organ
covered by epithelium,
that attaches the teeth to
the bones of the jaws and
provides a continually
adapting apparatus for
support of teeth during
function.
4 connective tissues

Two fibrous
- Lamina propria of
the gingiva.
- Periodontal ligament
Two mineralized
-Cementum
-Alveolar bone
 Gingival Fibers
Gingival Fibers
Functions:
Brace marginal gingiva
firmly against the tooth
Rigidity to withstand
mastication.
 PERIODONTAL LIGAMENT
The pdl is approx 0.25mm
in width, soft richly vascular
and celluar connective
tissue that surrounds the
roots of the teeth.
The major component is a
network of parallel
collagenous fibres inserting
into the cementum of the
root surface and lamina
dura. The other components
are cellular elements and the
tissue fluids. Blood vessels
and nerve endings
(proprioception) are also
found.
 Periodontal Ligaments
PDL supplied two kind nerve terminals (Burstone,1962)*
Ruffinni like endings
Nociceptive endings
Their importance in orthodontic is that Mechanorecptors are present in
apical region of root have a low thresholds and respond to minor
stretching of the PDL.
Nociceptors have a high threshold and thus
are activated by heavy by heavy force, tissue injury and inflammatory
mediators
These terminals changes their structures in response to an external
stimulus such as the application of orthodontic forces
Orthodontic movement affects the number, functional and distribution
of both mechanosensetive and nociceptive periodontal nerve fibers

*From text book on Biological mechanisms of tooth movement By V.

Krishnan and Z. Davidovitch first edition2009 page 60
 Principle Fibers of the
Periodontal Ligament
:
AC - alveolar crest fibers
H - horizontal fibers
OBL - oblique fibers
PA - periapical fibers
IR - interradicular fibers
These fibers are
remodeled by the
periodontal ligament
cells to adapt to
physiological needs
and respond to
different stimuli*
*Carranzas Clinical Periodontology 9th Edition
 Cementum
Cementum:
The calcified
avascular
mesenchymal
tissue that form the
outer covering of
the anatomic root.
Two main Types:
acellualr (primary).
cellular (secondary)
ACEL - acellular cementum; C crown; CC - coronal cementum
CEL - cellular cementum; CVX cervix; D dentin; E - enamel
R root; RC - radicular cementum

Carranzas Clinical Periodontology 9th Edition

 Cementum
Acellular cementum: Cellular cementum:
First to from. Formed after tooth
Formed before tooth reaches occlusal
reaches occlusal
plane. plane.
Covers cervical half of Covers apical half of
root. root.
Structure: Structure:
No cells.
Cementocytes
Sharpeys fibers
predominant. Calcified, (within lacunae).
Intrinsic collagen fibrils, Less calcified than
calcified, irregularly cellular cementum.
arranged and run Less Sharpeys fibers.
parallel to tooth surface

Carranzas Clinical Periodontology 9th Edition

 Cementum
Structure:
Collagen fibers:
Type I, III.
Two sources:
Sharpeys (extrinsic) fibers (embedded portion of
PDL); produced by PDL fibroblasts.
Fibers belong to cementum matrix per se (intrinsic);
produced by cementoblasts.
Cells:
Cementoblasts.
Cementocytes.
Organic matrix: produced by cementoblasts
Glycoproteins: BSP, osteopontin, tenascin, fibronectin,
osteonectin.
GAGs: hyaluronate, dermatan sulfate, chondroitin
sulfate. Keratan sulfate.
Proteogycans: syndecan lumican.
Inorganic matrix:
Hydroxyapatite.
 Alveolar Bone
Alveolar bone:
the portion of the
maxilla and mandible
that forms and support
the tooth sockets.
It forms when tooth
erupts and disappears
gradually after tooth
loss.
Provides osseous
attachment to the
forming PDL

Carranzas Clinical Periodontology 9th Edition

 Alveolar Bone
Consists of:
External plate of cortical
bone formed by
haversian bone and
compacted bone
lamellae.
Inner socket wall of thin,
compact bone called the
alveolar bone proper,
which conatins a series
of openings (cribrifirm
plate)
Cancellous trabeculae,
between the two
compact layer, act as
supporting alveolar bone
.
Carranzas Clinical Periodontology 9th Edition
 During normal function
During mastication the teeth and periodontal structures are subjected
to intermittent heavy forces. The tooth contact last 1second or less
during this forces are quit heavy which ranges from 1kg or 2kg or
50kg for soft and hard food substance respectively.

Little of the fluid with in the PDL space is squeezed out during the first
second of pressure application, if the pressure is maintained the fluid
is rapidly expressed, and tooth displaces with in the PDL space and
pain occurs after 3 to 5 seconds which indicates the fluid are
expressed and a crushing pressure is applied against the PDL within
the period.

Prolong force of low magnitude is produces a different physiological

response such as bone remodeling of the adjacent bone.

The orthodontic movement is made possible by application of

prolong forces

Also the natural environmental forces from lips cheeks or tongue

resting against the teeth have the same potential as orthodontic
forces
Proffitto
WRcause teeth to move basis
(ed) (2007)biological in different locations,
of orthodontic therapy : In
Contemporary orthodontic, 4th edn. Mosby, St louis
Proffit WR (ed) (2007)biological basis of orthodontic therapy : In
Contemporary orthodontic, 4th edn. Mosby, St louis
Proffit WR (ed) (2007)biological basis of orthodontic therapy : In
Contemporary orthodontic, 4th edn. Mosby, St louis
 Continuous Tooth Eruption

According to this concept eruption

does not cease when teeth meet their
functional antagonist s but continuous
throughout life. It consist of
-Active Eruption is the movement of the teeth in
the direction of occlusal plane
-Passive Eruption is the exposure of the teeth by
apical migration of gingiva

Carranzas Clinical Periodontology 9th Edition

 Orthodontic tooth
movement
This type of tooth movement can
occur rapidly or slowly, depending on
the physical characteristics of the
applied force and the size and the
biological response to periodontal
ligament. The forced induced strain
alter the PDL s vascularity and blood
flow, resulting in local synthesis and
various key molecule .
 Orthodontic vs. Orthopedic
Orthodontic forceforces
Force of higher
has been defined as
force applied to
teeth for the purpose
of effecting tooth
movement, generally
having a magnitude
lower than an
orthopedic force,
magnitude in relation
to an orthodontic
force, when delivered
via teeth for 12 to 16
hours a day, is
supposed to produce
a skeletal effect on
the maxillofacial
complex

Daskloginnakis(2000) Glossary of orthodontic terms Quintessence

Publishing
Kishnan , Berlin
V, Davidovitch Z (2006) The Cellular , molecular and tissue
level reaction to orthodontic forces. American Journal of Orthodontic
and dentofacial orthopedics ,129,e1-32
 Optimal Orthodontic force
It is defined as the Mechanical input
that leads to maximum rate of tooth
movement with minimal irreversible
damaged to the root, periodontal
ligament and alveolar bone

Daskloginnakis(2000) Glossary of orthodontic terms Quintessence

Cellular and molecular biology: Major determinants
of the outcome of orthodontic treatment

Cell biology related to orthodontic tooth movement

identified the Osteoblast cells as the cells that
control both the resorptive formative phases of the
remodeling cycle
Receptor studies have proven that these cells are
target for resorptive agents in bone as well as for
mechanical load.
Efforts are being made to identify specific molecule
involved in tissue remodeling during tooth
movement have unveiled numerous components
of cell nucleus cytoplasam and plasma membrane.
 Cellular and molecular
biology
The Receptor activator of nuclear factor kappa
B ligand (RANKL) and is decoy receptor and
Osteoprotegerin (OPG) are found to play
important roles in the regulation of bone
metabolism.
RANKL Promotes osteoclastogenesis
Osteoproteger inhibits its effect
Their expression was measured by Zhang et al
(2004)
In human PDL cells that were cultured for 6days
in the presence or absence of vitamin D3 , a
hormone that evokes bone resorption.
 Role of RANKL and OPG
The presence of RANKL in Vivo in compressed PDL was
demonstrated by immunochemistry .
(Kim et al) 2007
In a 55day old rat maxillary molar were moved laterally for 1-7
days . This movement was accompanied by findings of
positive staining for RANKL in the PDL cells paved way to
suggest that is responsible for bone resoption.
To inhibit ostoclast differentiation has led to attempt to inhibit
this reaction in order to prevent teeth from being moving
OPG plasmid was injected into the palatal PDL of the
maxillary first molar of rats undergoing orthodontic tooth
movement. The local gene trans fer induced OPG production
thus inhibiting osteoclastogenesis, and reducing tooth
movement.( Kanazaki etal 2004 Journal of dental research)
 Studies in the early 20th century
attempted mainly to analyze the
histological changes in paradental
tissues after tooth movement. Those
studies showed extensive cellular
activities in the mechanically
stressed PDL involving fibroblasts,
endothelial cells, osteoblasts,
osteocytes,and
Kishnan endosteal
V, Davidovitch Z (2006) cells and tissue
The Cellular , molecular
level reaction to orthodontic forces. American Journal of Orthodontic
and dentofacial orthopedics ,129,e1-32
Theories Of Orthodontic Tooth
Movement
The pressure tension theory
The bone bending theory
Bioelectrical signals in orthodontic
tooth movement
Arachidnonic acid metabolites
The intracellular secondary
messenger system
 The pressure tension theory

This is a classic theory of tooth

movement, here it relies on chemical
rather than electric signals as the
stimulant for cellular differentiation
and ultimately tooth movement.

Proffit WR (ed) (2007)biological basis of orthodontic therapy : In

Contemporary orthodontic, 4th edn. Mosby, St louis
The pressure tension theory
Classic histological research about tooth movement by
Sandstedt (1904), Oppenheim (1911), and Schwarz (1932)
led them to hypothesize that a tooth moves in the
periodontal space by generating a pressure side and a
tension side.

This hypothesis explained that, on the pressure side, the PDL

displays disorganization and diminution of fiber production.
There, cell replication decreases seemingly due to vascular
constriction.
On the tension side, stimulation produced by stretching of PDL
fiber bundles results in an increase in cell replication This
enhanced proliferative activity leads eventually to an
increase in fiber production
 First Histological Experiment
Sanstedt (1904)
In Sandstedts experimental model, a labial arch was bent to
engage the six maxillary incisors of a dog and inserted into
horizontal tubes attached to bands on the canines
The appliance was activated over a 3-week period by screws
distal to the buccal tubes and during that time the crowns of
the incisors were moved lingually by 3 mm.
Sandstedt found that bone was deposited on the alveolar wall
on the tension side of the tooth with both heavy and light
forces, and that the newly formed bone spicules followed the
orientation of the periodontal fiber bundles. On the pressure
side, with light forces, alveolar bone was resorbed directly by
numerous multinucleate osteoclasts in Howships lacunae
.With heavy forces, the periodontal tissues were compressed,
leading to capillary thrombosis, cell death, and the production
of localized cell-free areas of what he called hyalinization
(owing to its glasslike appearance resembling hyaline
cartilage in histological sections).

The tissue, cellular, and molecular regulation of orthodontic tooth movement: 100 years after Carl
Sandstedt
With heavy forces, the periodontal tissues were
compressed, leading to capillary thrombosis, cell death,
and
the production of localized cell-free areas of what he
called
hyalinization (owing to its glasslike appearance
resembling
hyaline cartilage in histological sections). At these sites,
osteoclastic resorption of the adjacent alveolar wall did
not take place directly, but was initiated by a process
referred
to by Sandstedt as undermining resorption from the
neighboring marrow spaces.
The tissue, cellular, and molecular regulation of orthodontic tooth
movement: 100 years after Carl Sandstedt
Murray C. Meikle European Journal of Orthodontics 28 (2006) 221240
Sandstedts histological findings following the application of a light force to the upper
incisors
of a dog; tooth cut in cross-section. (Left) Pressure side. Z, root surface; P, compressed
periodontal ligament; R, resorptive bone surface with numerous osteoclasts in
Howships lacunae; K, old alveolar bone with Haversian systems with no evidence of
bone transformation as described by Oppenheim. (Right) Tension side. Z, root surface
showing dentine and cementum; P, periodontal ligament; T, new bony trabeculae
orientated along the principal fi bres of the ligament; G, junction between new bone
and old compact bones, K. (From Schwarz, 1932 , International Journal of Orthodontia,
Schwarz (1932) detailed the concept further, by
correlating the tissue response to the magnitude of
the applied force with the capillary bed blood
pressure. He concluded that the forces delivered as
part of orthodontic treatment should not exceed the
capillary bed blood pressure
(20-25 g/cm2 of root surface).
If one exceeds this pressure, compression could cause
tissue necrosis through suffocation of the
strangulated periodontium. Application of even
greater force levels will result in physical contact
between teeth and bone, yielding resorption in areas
of pressure and undermining resorption or
hyalinization in adjacent marrow spaces
 Response to forces
Light, continuous Heavy, continuous
forces forces
Osteoclasts formed Blood supply to PDL
occluded
Removing lamina dura Aseptic necrosis
Tooth movement PDL becomes
begins hyalinized
Rlatively pain less HYALINIZATION
This process is called This process is called
FRONTAL UNDERMINING
RESORPTION RESORPTION.
 LIGHT forces leading to FRONTAL
RESORPTION
Phase 1 Mechanical compression and tension of the
periodontium
Phase 2 --- Mechanically induced cellular and genetic
responses; no tooth movement
Phase 3 --- Accelerated tooth movement due to frontal bone
resorption
Tooth movement (mm)

Phase 3
Phase 2
Phase 1

Time (Arbitrary Unit)

Frontal Resorption because it occurs
between the root and the lamina dura
 Undermining resorption because it occurs on the
underside of lamina dura, not between lamina dura and
the root.
 Another Histological study
Oppenheim (1911 , 1930 ) published the results of
experimental work carried out on the primary teeth of
Baboon. His observations proved to be substantially
different from those of Sandstedt as far as the response of
the bone to compression was concerned. He found that
where a tooth had been tipped labially, the original bone
disappeared completely from the labial surface and was
replaced by new bone.
He concluded that bone tissue, be it compact or
cancellated, reacts to pressure by a transformation of its
entire architecture; this takes place by resorption of the
bone present and deposition of new bone tissue; both
processes occur simultaneously. Deposition finally
preponderates
Tissue overresorption
changes, particularly of the bone, incident to
tooth movement
Albin Oppenheim
Vienna, Austria
(Transactions of the European Orthodontic Society 1911, pp. 303359)
 In 1930, Oppenheim republished his
earlier research on tooth
movement (which had been illustrated by
drawings and criticized as such)
together with the original
photomicrographs.

This is Figure 1 from the paper

showing (A) the original drawing and (B)
the photomicrograph of the bone
changes following labial movement of a
lower incisor for 40 days; tooth
sectioned vertically.
osteoclasts ( ok ) are absorbing bone on
the inner wall, simultaneous formation
of new bone is under way on the opposite
side of the process. At ob , near the
crest of the alveolus, compact bone has
disappeared and has been replaced
by cancellous bone; the trabeculae of the
latter have been arranged
perpendicular to the long axis of the
tooth; k 1 , new bone trabeculae lined
with osteoblasts ( ob ). (From Oppenheim,
1930 , International Journal of
Orthodontia, Oral Surgery and
Radiography.)
 Bone Bending Theory
Farrar was the first to suggest, in 1888, that alveolar bone
bending plays a pivotal role in orthodontic tooth
movement. This hypothesis was later confirmed with the
experiments of Baumrindin rats and Grimmin humans.
According to these authors, when an orthodontic appliance is
activated, forces delivered to the tooth are transmitted to
all tissues near force application. These forces bend bone,
tooth, and the solid structures of the PDL. Bone was found
to be more elastic than the other tissues and to bend far
more readily in response to force application. The active
biologic processes that follow bone bending involve bone
turnover and renewal of cellular and inorganic fractions.
These processes are accelerated while the bone is held in
the deformed position. These authors further stated that
reorganization proceeds not only at the lamina dura of
the alveolus, but also on the surface of every trabaculum
within the corpus of bone
Kishnan V, Davidovitch Z (2006) The Cellular , molecular and tissue level reaction to
orthodontic forces. American Journal of Orthodontic and dentofacial orthopedics ,129,e1-
32
 Dissipation of forces in bone
bending theory
The force delivered to the tooth is dissipated
throughout the bone by development of stress
lines, and further force application becomes a
stimulus for altered biological responses of
cells lying perpendicular to the stress lines.
The altered activity of cells in turn modifies the
shape and internal organization of bone, to
accommodate the exogenous forces acting on it.
This theory helps in gaining support for the Wolffs
law
Kishnan V, Davidovitch Z (2006) The Cellular , molecular and tissue level
reaction to orthodontic forces. American Journal of Orthodontic and
 Bioelectric signals in
orthodontic tooth movement
In 1962, Bassett and Becker28
proposed that, in response to applied
mechanical forces, there is
generation of electric potentials in
the stressed tissues. These potentials
might charge macromolecules that
interact with specific sites in cell
membranes or mobilize ions across
cell membranes.
 Electric current to accelarate
orthodontic tooth movement
It has been proposed by Davidovitch et al
that a physical relationship exists between
mechanical and electrical perturbation of
bone. Bending of bone causes 2 classes of
stress-generated electrical effects. Their
experiments with exogenous electrical
currents in conjunction with orthodontic
forces demonstrated enhanced cellular
activities in the PDL and alveolar bone, as
The objectives of this study were (1) to examine the usefulness of electric
currentswell as rapid
as a means tooth
to accelerate movement
orthodontic tooth movement in cats and
(2) to study the effect of a combined electric-orthodontic treatment on the
cyclic
Electric nucleotide profile
currents, bone remodeling, and tissue
and orthodontic turnover
tooth movement. Part-1 pattern
I1980 Jan (14 -of cat alveolar
32 ):Volume 77 bone and
Electric currents, bone remodeling, and orthodontic tooth movement
PDL.
II. Increase in rate of tooth movement and periodontal cyclic nucleotide levels by combined force and electric current
Zeev Davidovitch, D.M.D., Mathew D. Finkelson, B.S., Shulamit Steigman, D.M.D., Joseph L. Shanfeld, Ph.D., Paul C. Montgomery,
Ph.D., and Edward Korostoff, Ph.D.
 Zeev Davidovitch 1980
Applied electric currents to bone- 15 amps combined force
( 80 g)

Enhanced bone resorption near the anode & bone deposition

at the cathode compared to controls
Orthodontic tooth movement accelerated
 A word regarding
Piezoelectricity
Piezoelectricity is a phenomenon
observed in many crystalline
materials, in which a deformation of a
crystal structure produces a flow of
electric current as electrons are
displaced from 1 part of the lattice to
another. Apart from inorganic crystals,
it was found that organic crystals
could also exhibit piezoelectricity.
Such as hydroxiaptite,
 The 2 unusual properties of
piezoelectricity, which seem
to not correlate well with
orthodontic tooth movement
are

(1)a quick decay rate, where

the electron transfer from 1
area to another after force
application reverts back
when the force is
removed,which does not or
should not happen once
orthodontic treatment is
over; and
(2)production of an equivalent
signal in the opposite
direction upon force removal
Proffit WR (ed) (2007)biological basis of orthodontic therapy : In
Contemporary orthodontic, 4th edn. Mosby, St louis
 PHASES OF TOOTH
MOVEMENT
In 1962, Burstone suggested that, if
the rates of tooth movement were
plotted against time, there would be
3 phases of tooth movement
A. An initial phase,
B. A lag phase, and a
C. Post lag phase.
 The initial phase
The initial phase is characterized by
rapid movement immediately after
the application of force to the tooth.
This rate can be largely attributed to
the displacement of the tooth in the
PDL space.
 The initial phase
Cellular and tissue reactions start in the initial
phase of tooth movement, immediately after
force application. Because of the compression
and stretch of fibers and cells in PDL pressure and
tension areas, respectively, the complex process
of recruitment of osteoclast and osteoblast
progenitors, as well as extravasation and chemo
attraction of inflammatory cells, begins. The
presence of hyalinized zones in the pressure area
was demonstrated in recent experiments even in
this early stage
 Lag Period
After the initial phase, there is a lag period,
with relatively low rates of tooth
displacement or no displacement. It has been
suggested that the lag is produced by
hyalinization of the PDL in area of
compression. No further tooth movement
occurs until cells complete the removal of all
necrotic tissues. The third phase of tooth
movement follows the lag period , during
which the rate of movement gradually or
suddenly increases.
 In the second phase, areas of compression are easily recognized
by the distorted appearance of the normal PDL fiber arrangement.
The disruption in blood flow due to this distortion leads to the
development of hyalinized areas and the arrest of tooth
movement, which can last from 4 to 20 days. Only removal of
necrotic tissue and bone resorption from adjacent marrow spaces
(indirect resorption) and from the direction of the viable PDL
(undermining resorption) allow the resumption of tooth
movement. This comprehensive process requires the recruitment
of phagocytic cells such as macrophages, foreign body giant cells,
and osteoclasts from adjacent undamaged areas of the PDLand
alveolar bone marrow cavities. These cells act in tandem to
remove necrotic tissues from compressed PDL sites and adjacent
alveolar bone. In areas of PDL tension, quiescent osteoblasts
(bone surface liningcells) are enlarged and start producing new
bone matrix
 The third phase of tooth movement
follows the lag period , during which
the rate of movement gradually or
suddenly increases.
Arachnodic acid metabolites
Arachidonic (eicosatetraenoic) acid, the main component of
phospholipids of the cell membrane, is released due to the
action of phospholipids enzymes. The released acid can be
metabolized by 2 pathways
1 the cyclooxygenase pathway (with the help of
cyclooxygenase enzymes producing prostaglandins and
thromboxanes)
2 the lipooxygenase pathway leadingto release of leukotriens
(originally demonstrated in leucocytes with 3 double bonds
(trienes) in the backbone of the molecule) and
hydroxyeicosatetraenoic acids.
 Prostaglandins in tooth
movement
Von Euler, who first discovered the
compound inhuman semen and believed
the prostate gland to be the main source
of this chemical substance, introduced
the term prostaglandin. However, it was
later discovered that most cell types in
the body produce prostaglandins
Prostaglandins are important mediators
of mechanical stress
 Clinical application of PGE1 upon
orthodontic tooth movement
Yamasaki et al(1984)
Chemically produced-PGE1 was
administered in clinical cases OTM

I phase- lingual arch springs

applied on both sides of the
maxilla to upper I premolars
- scheduled for extraction.

One side - submucosal

injections of PGE1 and the other
side -vehicle injections.

The rate of tooth movement in

buccal direction doubled on the
side of several PGE1 injections
as compared to the control side.

1984 Jun (508 - 518): Clinical application of prostaglandin E1 upon orthodontic tooth movement - Yamasaki, Shibata,
Imai, Tani, Shibasaki, and Fukuha
 Yamasaki et al(1984)
2nd phase- PGE1
injections in canine-
retraction cases for 3
weeks were I premolar-
extraction was done -
(sectional contraction
loops)
Rate of distal canine
movement-almost
double on the side
receiving PGE1 injections
as compared to the
vehicle-injected side.

1984 Jun (508 - 518): Clinical application of prostaglandin E1 upon orthodontic tooth
movement - Yamasaki, Shibata, Imai, Tani, Shibasaki, and Fukuha
 Yamasaki et al(1984)
3rd phase- PGE1 injections applied
on routine canine retraction in I
premolar-extraction cases.
Rate of distal canine movement was
almost 1.6-fold on the side of PGE1
injections as compared to the vehicle-
injected side.
Throughout the study, no side
effects were observed
macroscopically in the gingiva and
roentgenographically in the
alveolar bone, except for slight pain -
consistent with orthodontic tooth
movement
 The intracellular second-
messenger systems
Sutherland and Rall established the Second-messenger
basis for hormone actions in 1958. discovered that free
glucose appeared in the bathing media of liver slices
exposed to adrenaline. They proposed that the first
messenger (a hormone or another stimulating agent)
binds to a specific receptor on the cell membrane and
produces an intracellular chemical second messenger.
This second messenger then interacts with cellular
enzymes, evoking a response, such as protein
synthesis or glycogen breakdown. Two main second-
messenger systems are now recognizedthe cyclic
nucleotide pathway and the phosphatidyl inositol (PI)
dual signaling system.
 PATHWAYS OF TOOTH

MOVEMENT
On the basis of research in basic biology and
clinical observations, Mostafa et al proposed an
integrated hypothetical model for tooth
movement. This model consists of 2pathways
I and IIthat work concurrently to induce
tooth movement. According to these authors
pathway I represents the more physiologic
response, because it is usually associatedwith
normal bone growth and remodeling.
pathway II represents the generation of a local
inflammatory response by orthodontic forces.
1983 Mar (245 - 250): Orchestration of tooth movement - Mostafa,
Weaks-Dybvig, and Osdoby
 Recent model Jones et al
1991
It is based on the assumption that stress in any formcompressive, tensile, or shear
will evoke many reactions in the cell, leading to the development of strain.
In osteoblasts, the first measured responses to physiologic levels of stress are
increases in intracellular free calcium and membrane potential through activation of
K channels.
This increase in calcium concentration is related to the activation of phospholipase
C, which releases inositol triphosphate within 10 seconds.
Elevated levels of phospholipase C maintain the high calcium concentration
throughout stress application by keeping the mechanosensitveion channels open and
by further activation of protein kinase C through diacylglycerol after 3 to 4 minutes
of force application.
Phospholipase A is activated; it acts on stores of arachidonic acid, leading to
detection of prostaglandins in the culture medium after about 10 minutes.

This event is followed by the release of products of the lipooxygenase pathway

(leucotriens and hydroxyeicosatetraenoic acids), followed by an elevation in the
concentration of cAMP. The phosphorylation reactions mediated by this cyclic
nucleotide in the nucleus and the cytoplasm lead to cellular syntheticand secretory
activities.
 Cellular & Molecular
mechanism
Cell membrane perturbation Periodontal
vascular change
Transduction Membrane
by integrins phospholipids
Stretch activated
ion channels
Cytokines

Receptor
Ca 2+

cAMP

Transcription factors Activate/repress genes

66
 Mechanotransduction
Mechanosencing is postulated to involve many
different cellular and extracellular components .
Mechanical forces cause direct stretching of
protein surface integrin binding sites that occur
on all eukaryotic cells. Stress induced
conformational changes which leads to several
secondary messenger pathways leading to
altered regulation of genes that synthesize and
catabolize extracellular matrix protein, as well
as to alter cell division

Textbook- Biological mechanism of tooth movement by Krishnan and

Davidovitch 2009
 Mechanotransduction
It is believed that mechanical adaption is
governed by osteo cytes which respond to
a loading induced flow of interstitial fluid
through the lacuno-canaliculular network
by producing signaling molecules
Bone cells are highly responsive to
mechanical stimuli, but critical component
s in the loading profile is still not clear

Textbook- Biological mechanism of tooth movement by Krishnan and

Davidovitch 2009
Mechanism of conversion:
Mechanical force - cellular
change
FORCE

STRAIN ON THE CELLS/CHANGE IN THE VASCULAR FLOW

CHEMICAL MESSENGERS

ACT ON CELLS- SECOND MESSENGERS

INDUCE TRANSCRIPTION FACTORS

GENETIC CODING - PHENOTYPIC CHANGE

70
 Mechanical stress resulting in tissue
deformation can be concentrated in certain
regions in tissue like muscle attachment
sites, ligament blood vessels bone matrix
The deformation involves the cells with in
resident and on matrix surface enticing them
to direct structural changes which respond
very efficiently i.e. straining on one side and
at the same time cells detect lowering of
strains on the compression side. Therefore
increased secretion of prostaglandin
elevation of cyclic nuceotides and change in
fluid flow and streaming potential

Textbook- Biological mechanism of tooth movement by Krishnan and Davidovitch

2009
 Integrins
Conversion of mechanical force-
OTM-interplay between intra-
extracellular elements
Integrins (Microfilaments)
ECM
Cytoskeleton
(collagen,fibronectin,laminin)

Cytokines
Released
72
 Integrins
Microfilaments+ ECM Junctional
complex-Focal adhesions
 The relationship of nerves to tooth movement
Mechanoreceptors in the apical half of root-
Raffini & Nociceptive
Force sensing fibres
(unmyelinated c fibres/ myelinated A)

Nerve terminal strained

Stored neuropeptides released

Substance P, Vassoactive intestinal IP, CGRP

PG E2 & cAMP
 EXTERNAL APICAL ROOT
RESORPTION
The first orthodontists to describe the
association between treatment and
resorption, Ottolengui,1914 and
Ketcham1927 noted that of the several
possible modes of movement, intrusion
and heavy tipping forces are the most
likely to cause noticeable apical
resorption. Intrusion damages the root
apex because root shape concentrates
pressure at the conical root tip
Shaza K. Abass and James K. HartsField, Jr Seminars In
Orthodontics,Vol13,No 4 (December), 2007
 Root Resorption
Root resorption can be classified into
at least 3 categories
1.Surface resorption
2.Inflammatory resorption
3.Replacement resorption

Shaza K. Abass and James K. HartsField, Jr Seminars In

Orthodontics,Vol13,No 4 (December), 2007
 Surface resorption
Surface resorption occurs constantly as
microdefects on all roots. These normally
repair themselves without notice. It is
only consequential when lacunae in the
cementum broaden and permit
dentinoclasia. Surface resorption can
occur anywhere on a root but is most
common periapically. Surface resorption
stops when the instigating agent (usually
pressure) is removed and there is repair
of the cementum
 Inflammatory resorption
Inflammatory resorption occurs when
root resorption progresses into the
dentinal tubules to pulpal tissue that
is infected or necrotic or into an
infected leukocyte zone

Shaza K. Abass and James K. HartsField, Jr Seminars In

Orthodontics,Vol13,No 4 (December), 2007
 Replacement resorption
Replacement resorption produces
ankylosis of a tooth because bone
replaces the resorbed tooth
substance

Shaza K. Abass and James K. HartsField, Jr Seminars In

Orthodontics,Vol13,No 4 (December), 2007
In most of the reports, resorption occurred mainly in the
apical third of the root .Two possible explanations for
theThe
1. fulcrum
increased is occlusal
incidence to the apical
of resorption half in
lacuna of the
thethird
apical root were:
and the differences in the direction of the
periodontal fibers could result in increased
possibilities of trauma in the apical and middle
thirds of the root.
2. The apical third is covered with cellular cementum
while the middle and gingival thirds are covered
with acellular cementum. The cellular cementum
depends on more active cells, and has more
supporting vasculature,which makes it more liable
to trauma and cellinjury reactions.
 According to Proffit
1) Moderate Generalized-
-long Rx duration

2) Severe Generalized
-evidence of resorption before Rx
-etiology

3) Severe Localized-
-may be caused due to orthodontic Rx-cortical plates
 Mechanism of root resorption

Orthodontic force transmitted to the periodontal ligament

(PDL) is subjected to the mechanical
forces of compression and tension.

In cases of heavy forces over long durations the PDL is injured

resulting
in hylanized tissue formation

Remodeling of the periodontal

ligament as a result of its injury and necrosis

Shaza K. Abass and James K. HartsField, Jr Seminars In Orthodontics,Vol13,No 4

(December), 2007
 First cells that appear in the necrotic area are
macrophages which are responsible for the initial
resorption of the pre-cementum
layer

later followed by multinucleated cells (odontoclasts),

which attack cementum and eventually dentin.

Removal of the hylanized tissue leads also to the

removal of the cementoid layer, which is believed to be
a protective layer

This process might leave a raw surface of cementum

that can be readily attacked by odontoclasts . Thus
cousing root resobtion
Shaza K. Abass and James K. HartsField, Jr Seminars In Orthodontics,Vol13,No 4
(December), 2007
 Measurement Methods
EARR can be defined operationally as
the degree a root has shortened from its
original (or expected) length by clastic
activity. Broadly, two methods have
been used to quantify resorption:
1.Visually-assessed grades of resorption
2.Computer-aided device (ratio scale
data),almost always on radiographs.
Levander & Malmagren-scoring
criteria

Shaza K. Abass and James K. HartsField, Jr Seminars In

Orthodontics,Vol13,No 4 (December), 2007
 Factors effecting root
resorption
Biologic factors-
Individual susceptibility- major factor- variation
in the pattern of metabolic signals
Age- Poor correlation
Higher susceptibility in adults- PDL changes
Sameshima & Sinclair- inc. resorption of mandibular
anteriors-adults
Incidence inc with age as vascularity dec & bone
density inc
Masseler & malone- even without tmt- resorption
more as age inc

Gender-Lack correlation- conflicting results

Females may be more suseptible(3.7:1)-males
are chronologically younger
Sameshima & Sinclair- males- more prone- not 88
Effect of Pharmacological
Agents
on Root Resorption
Molecules that affect osteoclast activity
negatively such as bisphosphonates have
the potential to reduce root resorption,
but also reduce tooth movement.
The administration of echistatin, an
arginineglycine-aspartate acid (RGD)-
containing peptide was found to be
effective in reducing root resorptionduring
tooth movement in rats
Effect of Pharmacological
Agents
on Root Resorption
The administration of corticosteroids in
doses
of 15 mg/kg to rats during orthodontic
treatment increased root resorption,
whereas low doses of 1 mg/kg decreased
root resorption.
Doxycycline, a potent collagenase inhibitor,
is capable of reducing the number of
osteoclasts and preventing root resorption
and alveolar bone loss following
mucoperiosteal flap surgery in rats
Effect of Pharmacological
Agents
on Root Resorption
The administrationof very low doses of L-
thyroxin was shown to decrease root
resoption in both rats and human studies.
It is assumed thyroxin either increases the
resistance of the cementum and dentin to
clastic activity or increases the rate of alveolar
bone resorption. It is well documented that
thyroid hormone exerts a biphasic effect on
bone formation and resorption. At lower doses
it may increase bone formation,whereas at
larger doses bone resorption is enhanced
 Repair of Root
Resorption
The idea that roots of permanent
teeth are repaired after mechanical
damage was first introduced into
literature by Bridgman in 1862
A detailed histological picture of
repair was first reported by Fletcher
in 1911.

Shaza K. Abass and James K. HartsField, Jr Seminars In

Orthodontics,Vol13,No 4 (December), 2007
 Brudvik and Rygh have shown that resorptive
areas are repaired by deposition of cementum
and further reestablishment of the periodontal
ligament. In a study on human premolars using
light microscopy and scanning electron
microscopy, Langfordand Sims have shown that
repair occurs entirely with cellular cementum.
They have also shown the presence of Sharpey
fiber holes in the new cementum, indicative of
principal periodontal fiber insertion and PDL re-
establishmentat that site. Although it has been
proposed that small areas of resorbed
cementum will typically be repaired, if the
resorption exceeds reparative capacity at the
apical end of the tooth, the root is shortened
Effect of Systemic Drugs
and Diseases On
Orthodontic Tooth
Movement
 diseases on
orthodontic tooth
Introduction movement
Tissue systems of particular importance in
orthodontics are the nervous, vascular,
immune, endocrine, and skeletal systems.
Drugs aimed at any of these systems may
reach the mechanically stressed PDL, interact
with local target cells, and modify their
reactions to the applied force. To avoid
undesirable influences on tooth movement, the
orthodontist should be aware of any drugs
taken by each individual patient
Krishnan V, Davidovitch Z : The effect of drugs on orthodontic tooth movement Orthod Craniofacial Res 9,
2006; 163171
 Non-steroidal anti-
inflammatory drugs
The most common group of medications used in day
to day basis for pain relief which consists of non-
steroidal anti-inflammatory drugs
They functioning by inhibition of the enzyme
cyclo-oxygenase (COX), which modulates the
transformation of prostaglandins (PGs) from
arachidonic acid in the cellular plasma membrane
NSAIDs effectively reduce pain and discomfort
caused by the periodic activation of orthodontic
appliances, but that these drugs may also affect the
sequence of tooth movement by inhibiting, or at
least by reducing the associated inflammatory and
bone resorptive processes
Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth movement Orthod Craniofacial Res 9,
 Role of NSAID
When NASID were administered it was seen that
levels of matrix metalloproteinase (MMPs)-9 and
-2 were found to be increased, along with
elevated collagenase activity, followed by a
reduction in pro-collagen synthesis, which are
considered essential as far as bone and
periodontal ligament remodeling is considered.
The whole process is thought to be the result of
inhibition of COX activity, leading to altered
vascular and extracellular matrix remodeling,
causing reduction in the pace of tooth movement

Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth

movement Orthod Craniofacial Res 9, 2006; 163171
Drugs used in Osteoporosis
It is a condition resulting in a loss of
bone mass and strength, a decrease
in bone turnover with increased
resorptive activity, found
predominantly in post-menopausal
women, but also in adult males

Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth movement

Orthod Craniofacial Res 9, 2006; 163171
 Most of the approved osteoporotic
drugs are anti-resorptive, slowing
down the destructive phase
(resorption) of bone turnover. The
anti-resorptive medications
commonly used by osteoporotic
patients include :-Bisphosphonates
estrogen, selective estrogen receptor
modulators, and calcitonin
Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth movement Orthod
Craniofacial Res 9, 2006; 163171
 These drugs and hormones produce
modest increases in bone density,
with the help of increases in the
mineralization of old bone.
These drugs have reported to
reduced root resorption without
significant influence on the alveolar
bone.
Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth
movement Orthod Craniofacial Res 9, 2006; 163171
 Drugs used in Rheumatoid
arthritis
Rheumatoid arthritis (RA) is
characterized by the presence of
immune-mediated inflammatory
synovitis that exhibits the capacity to
invade and destroy the extracellular
matrices of joint cartilage and bone

Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth movement

Orthod Craniofacial Res 9, 2006; 163171
 Most the drugs used for treatment of RA include
immuno-modulatory agents TNF antagonists or
interleukin antagonists .The immuno-modulatory
drugs modulates nuclear factor kappa B,
tyrosine kinases in the signaling pathway,
interleukin 6,MMPs and PGE2, all of which are
essential for the bone remodeling process TNF
alpha antagonists will block TNF alpha in
inflammatory cytokines released by activated
monocytes, macrophages and T-lymphocytes,
which are essential for inflammatory responses
following force application . Thus reducing the
pace of bone remodeling and there by slowing
tooth movement.

Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth

movement Orthod Craniofacial Res 9, 2006; 163171
Immunosuppressant drugs
These drugs produces pronounced or severe
gingival hyperplasia, making orthodontic
treatment, as well as maintenance of oral hygiene
difficult.
Orthodontic treatment should be deferred in
these patients. Treatment should be started or
resumed once oral hygiene is very good and after
surgical removal of excessive gingival tissue.
Whenever possible, fixed appliances should be
kept to a minimum period with only brackets, and
avoiding the use of cemented bands. Use of
removable appliances in these patients is not
recommended due to failure of proper fit
 Corticosteroid therapy
Recently expressed concern has been
about orthodontic treatment in patients
undergoing corticosteroid therapy for its
anti-inflammatory and
immunosuppressive effects. The cited
side effects of long-term steroid therapy
include disturbances in mineralized tissue
metabolism and wound healing,
discrepancies in chondrogenesis and
osteogenesis, bone loss and osteoporosis.
Krishnan V, Davidovitch Z The effect of drugs on orthodontic tooth movement
Orthod Craniofacial Res 9, 2006; 163171
 Corticosteroid therapy
Force application resulted in a
significant increase in the relative
extension of resorption and
formation in both groups, indicating
that the orthodontic force level
should be reduced and controlled
more frequently in patients on
chronic steroid treatment
 Drugs that promote or retard
orthodontic
tooth movement
Prostaglandins and analogs
Certain eicosanoids (PGs and leucotrienes) released
from paradental cells in sites of compression and
tension have significant stimulatory effects on bone
remodeling. This finding led researchers to inject
PGs locally at the site of orthodontic tooth
movement, to enhance the bone remodeling
process, and thereby enhance the pace of tooth
movement Yamakazi et al
found an increased number of osteoclasts in rats
alveolar bone after local injection of PGE1
 Effect of nicotine on
orthodontic tooth
movement
Nicotin is an alkaloid from the
oxygen-free alkaloid group, which is
the major psychoactive component
of cigarette smoke that is highly
addictive

Ahmad Sodagar March 2011 American Journal of orthodontics and dentofacial

 Nicotine causes an increase in the
expression of the cyclooxygenase-2 (COX-
2) gene and prostaglandin E2 (PGE2)
release in human gingival fibroblasts in a
time and dose-dependent manner. COX is
the main enzyme for converting
arachidonic acid to prostaglandins, which
are important factors in bone resorption.
Therefore, nicotine administrationmight
increase orthodontic tooth movement
 MATERIAL AND METHODS
Thirty-two adult male Sprague-
Dawley rats weighing250 20 g.
The rats were randomly divided into
4 equal groups:
3 experimental groups and 1
control group.
 With the rats under general anesthesia, 5-
mm nickel-titanium closed-coil springs were
placed between the maxillary right first
molars and first incisors. Injections of
nicotine (Nicotin tartate salt)were
administered daily for 13 days
Intraperitonealy
Group A, 0.5 mg per kilogram
Group B, 0.75 mg per kilogram
Group C, 1 mg per kilogram.
Group D, the control group, received
injections of 0.1 mL of normal saline
solution
 Fourteen days after appliance
placement, the animals were
anesthetized with ether.
In each rat, the amount of
orthodontic tooth movement
between the maxillary right first
molar and incisor was measured by
using aninterproximal feeler gauge
Result
 Several studies showed that nicotine
has direct effects on the small blood
vessels in causing vasoconstriction and
systemic vasoconstriction, which lead to
hypoxia. Based on the pressure-tension
theory, hypoxia in the pressure side
leads to chemical mediator production
that leads to osteoclast differentiation
and bone resorption. The hypoxia
caused by nicotine might contribute to
the production of chemical mediators in
the pressure side and accelerate bone
resorption and tooth movement
Results have shown acceleration of
orthodontic tooth movement with
nicotine, all of its
detrimental effects on health and highly
addictive features, and the dangerous
consequences of smoking,absolutely do
not rationalize smoking. We as an
Orthodontists, like other health care
professionals, should try to encourage
their patients to stop smoking.
Conclusion
We can all now say that the need to know
about the changes in orthodontic tooth
movement in molecular and in cellular
level that takes place while application of
orthodontic forces to move teeth in patient
, whose expression or inhibition can
increase or decreases or inhibit the speed
at which the tooth can be moved . This
knowledge will also determine if how long
the treated teeth will survive. The disorder
,trait and condition that will determine
which patient will be easier to treat, which
patient will require more work and which
patients should not be treated at all.